Biomedical subjects

J Represa

Publications and source records attributed to J Represa.

43 records · Page 3Linked to original sources

PubMed1991

Temporal pattern of nerve growth factor (NGF) binding in vivo and the in vitro effects of NGF on cultures of developing auditory and vestibular neurons.

NGF binding patterns reflect the presence of receptors for this growth factor. High specific binding of 125I 2.5 S-NGF was observed for the 11 gestation day (gd) statoacoustic ganglion (SAG) with lower levels recorded for both 14 gd acoustic ganglion (AG) and vestibular ganglion (VG) samples. Fourteen day AG cells were more than twice as active for binding NGF when compared to VG samples of the same gestational age. Both whole ganglion explants and dissociated cell cultures were grown in chemically defined medium for short term culture to assay changes in neurite outgrowth and survival of neurons in response to the addition of exogenous 2.5 S-NGF. The most vigorous neurite outgrowth and neuronal survival responses were produced by 11 gd SAG samples treated with NGF. Acoustic ganglion specimens of both 11 gd and 14 gd embryos were much more responsive to the neurotrophic effects of NGF when compared to the responses of their VG counterparts. There was a correlation between NGF binding ability and in vitro responsiveness to exogenous NGF. We hypothesize based on the results of this study that NGF (and/or a member of the NGF family of growth factors) is involved in the control of developmentally regulated neuronal cell death of SAG neurons and may play a role in the innervation of developing inner ear sensory structures.

Animals↗

PubMed1990

Retinoic acid modulation of the early development of the inner ear is associated with the control of c-fos expression.

The effects of retinoic acid (RA) on the early development of the inner ear were studied in vitro using isolated chick embryo vesicles. Low concentrations of RA (1-50 nM) inhibited vesicular growth in stage 18 otic vesicles that were made quiescent and then reactivated by either serum or bombesin. Growth inhibition was concentration-dependent and was paralleled by a reduction in the rate of DNA synthesis as measured by [3H]thymidine incorporation. Half-inhibition occurred between 1 and 10 nM RA, and the full effect at 20 nM. Retinoic acid, in the presence of serum, induced the precocious differentiation of (1) secretory epithelium, the tegmentum vasculosum and endolymphatic sac and (2) early sensory and supporting epithelia. These structures were positioned in their corresponding normal presumptive areas. The overall direction of growth was reversed by RA and the ratio of the internal to the external vesicular surface area increased with RA concentration. The expression of the nuclear proto-oncogene c-fos in the developing otic vesicle was transient and stage-dependent. High levels of c-fos mRNA were positively correlated with cell proliferation. Incubation of growth-arrested otic vesicles with bombesin plus insulin at concentrations that induced cell proliferation produced a strong induction of c-fos. This mitogen-induced expression was suppressed by 25 nM RA. The results suggest (1) a role for retinoic acid in controlling the early development of the inner ear and (2) that this control is effected through the regulation of the proto-oncogene c-fos.

Animals↗

PubMed1990

[Tumor markers in liver metastases of colorectal carcinoma].

Colorectal cancer is a potentially curable tumour when diagnosed in the early stages. In order to improve the results obtained up to now, we propose application of a diagnostic program among patients who undergo curative resection for colorectal adenocarcinoma, which would consist of using a panel of tumor markers, in combination with endoscopic, histologic and ultrasonographic diagnostic methods. For this study we studied 105 patients, divided into two groups: A) Group 1: 30 control patients. B) Group 2: 75 patients diagnosed as having colorectal cancer. We performed the preoperative determination of a series of tumor markers (CEA, CA 19.9, GGT and PHI), endoscopy/biopsy and hepatic ultrasonography on these patients. Our results suggest that the design of the preoperative diagnostic program makes early detection of hepatic metastases possible. The tumor marker panel combination provided a visible increase in sensitivity for detecting hepatic metastases.

Adenocarcinoma↗

PubMed1990

[The development of stria vascularis in the guinea pig fetus].

In the 25 day old guinea pig fetus the lateral wall of the ductus cochlearis is lined with a cylindrical epithelium consisting of a single layer of columnar cells, which opens onto the endolymphatic space. It is clearly separated from the adjacent structures by a basal membrane. This connective tissue contains numerous cells with fibroblastic features, more abundant and larger, the nearer they are to the basal membrane. In the segment of the marginal cells adjoining the endolymphatic cleft sometimes shows up a basal body, suggesting the existence of a kinocilium. The cellular surface is covered with small microvilli. In the 50 day old guinea pig fetus, the development of the stria vascularis is already similar to that of the adult animal.

Animals↗

PubMed1989

Characterization and localization of nerve growth factor receptors in the embryonic otic vesicle and cochleovestibular ganglion.

We have investigated the possibility that nerve growth factor (NGF) may play a role in the development of the inner ear. Primordia of the inner ear, the otic vesicle (OV) and cochleovestibular ganglion (CVG), were isolated from 72-hr (stage 19-20) quail embryos and examined for the presence of NGF receptors. Quantitative binding studies revealed that both OV and CVG exhibited specific 125I-NGF binding; levels of nonspecific binding were 6 to 26% of total binding. Scatchard analysis yielded a linear plot, indicating the presence of a single class of NGF receptor. The average binding constant (Kd) was 8.0 nM for OV and 8.6 nM for CVG, corresponding to the low affinity (site II) NGF receptor. Examination of light microscopic radioautographs indicated that most of the specific 125I-NGF binding was located in the ventromedial wall of the OV, with little or no binding in the lateral wall and endolymphatic primordia. These studies were corroborated by microdissection of OV, in which 70% of the radioactivity was found to be localized in the medial half of the OV. In CVG, specific 125I-NGF binding was more concentrated in the cochlear portion of the ganglion, with silver grains primarily over areas containing support cells and immature neurons. Quantitative binding studies with isolated cochlear and vestibular ganglia obtained from 144-hr (stage 29-30) quail embryos revealed that the cochlear ganglion exhibited three times more specific 125I-NGF binding than the vestibular ganglion. The presence of NGF receptors on OV and CVG suggests that these structures are responsive to and/or dependent upon NGF. The following paper (J. Represa and P. Bernd, 1989, Dev. Biol. 134) examines the question of whether NGF serves either as a mitogen, a survival factor, or a differentiation factor in this system.

Animals↗

PubMed1989

Nerve growth factor and serum differentially regulate development of the embryonic otic vesicle and cochleovestibular ganglion in vitro.

The preceding paper (P. Bernd and J. Represa, 1989, Dev. Biol. 134) describes the characterization and localization of nerve growth factor (NGF) receptors in inner ear primordia, the otic vesicle (OV) and cochleovestibular ganglion (CVG), obtained from 72-hr (stage 19-20) quail embryos. The studies described in this paper investigated whether NGF serves as a mitogen, a survival factor, and/or a differentiation factor in this system. Explants of isolated OV and CVG were maintained for 24 hr in serum-free medium alone (M-199), M-199 containing serum, M-199 containing NGF, or M-199 containing both serum and NGF. [3H]Thymidine was also present for the entire culture period. Both OV and CVG incorporated greater amounts of [3H]thymidine in the presence of serum or NGF, and their combined effect was additive. NGF's effects were dose dependent, saturable, and specific (blocked by anti-NGF). NGF caused little or no morphological differentiation of OV and no increase in protein levels, in contrast to OV grown in the presence of serum. CVG had both cochlear and vestibular portions present in all cases, but the apparent size and protein content of CVG was increased in the presence of either serum or NGF. Effects of serum and NGF were completely, but reversibly, blocked by amiloride, suggesting that the Na+-H+ exchange system had been activated. In order to determine whether increases in [3H]thymidine incorporation were due to increased cell survival or perhaps to an increase in proliferation, explants were initially grown for a 24-hr period in serum-free medium, followed by reactivation for an additional 24 hr in medium containing serum and/or NGF. It is likely that cells requiring either serum or NGF for survival would die during a 24-hr period in their absence. Our results revealed that the level of [3H]thymidine incorporation in OV was the same after reactivation. In the case of CVG, only NGF treatment yielded similar results; [3H]thymidine incorporation was lower in CVG reactivated with serum. It appears, therefore, that serum has probable proliferative effects upon OV and CVG, as well as survival effects for CVG. NGF, however, does not appear to affect survival in either OV or CVG, so that increases in [3H]thymidine incorporation in response to NGF are most likely due to proliferative effects upon OV or CVG, at least at this embryonic stage.

Amiloride↗

PubMed1989

Mesoderm induction by the mesoderm of Xenopus neurulae.

Combinations were made between explants of mesoderm from the archenteron roof of early Xenopus neurulae and explants of ectoderm from mid-blastulae. In each combination one component was labeled with the fluorescent lineage label RDA (rhodamine-dextran-amine). Frequent and large mesoderm inductions, consisting mainly of muscle, were found where the presomite plate was used as the inducer. Less frequent and smaller mesoderm inductions were found when notochord was used as the inducer. We conclude that induced mesoderm can itself be active as a mesoderm inducing tissue. If this capability is acquired in the blastula then it follows that mesoderm induction must propagate from cell to cell and its spread be antagonized by some other factor.

Animals↗